Affiliation: Memorial Sloan-Kettering Cancer Center
- Factor V Leiden mutation investigated by amplification created restriction enzyme site (ACRES) in PNH patients with and without thrombosisK Nafa
Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 0021, USA
Haematologica 81:540-2. 1996..Fifty-six PNH patients were tested for Factor V Leiden mutation using Amplification Created Restriction Enzyme Site methods. PNH patients do not show an increased frequency of Factor V Leiden mutations...
- The spectrum of somatic mutations in the PIG-A gene in paroxysmal nocturnal hemoglobinuria includes large deletions and small duplicationsK Nafa
Department of Human Genetics, Memorial Sloan Kettering Cancer Center, NY, New York 10021, USA
Blood Cells Mol Dis 24:370-84. 1998..The increasing number of identified missense PIG-A mutations should help elucidate structure-function relationships in the PIG-A protein...
- New somatic mutation in the PIG-A gene emerges at relapse of paroxysmal nocturnal hemoglobinuriaK Nafa
Department of Human Genetics, Memorial Sloan Kettering Cancer Center, New York, NY, USA
Blood 92:3422-7. 1998..These findings support the notion that the BM environment may create selective conditions favoring the expansion of PNH clones...
- Cytogenetic and morphological abnormalities in paroxysmal nocturnal haemoglobinuriaD J Araten
Department of Human Genetics, Memorial Sloan-Kettering Cancer Center, New York, USA
Br J Haematol 115:360-8. 2001..However, none of our patients developed excess blasts or leukaemia. We conclude that in patients with PNH cytogenetically abnormal clones are not necessarily malignant and may not be predictive of evolution to leukaemia...
- Association of clonal T-cell large granular lymphocyte disease and paroxysmal nocturnal haemoglobinuria (PNH): further evidence for a pathogenetic link between T cells, aplastic anaemia and PNHA Karadimitris
Department of Human Genetics, Memorial Sloan-Kettering Cancer Center, New York, NY, USA
Br J Haematol 115:1010-4. 2001..Thus, T-LGL clones in AA, MDS and PNH probably expand as a result of antigenic stimulation. It is postulated that the antigen driving clonal T-cell proliferations in these disorders exists on haemopoietic stem cells...